As both men and mice age, their immune systems lose their ability to function normally. My objectives are to measure in mice the amount of immune functional loss that is intrinsically timed within (1) immune precursor cell lines, or (2) immune organ microenvironments, and (3) the amount of loss due to inadequate support of immune activity in the aged mouse's deficient internal environment. In the first objective, immune precursor cells from aged donors will be transferred to young recipients. The immune responses of aged compared with younger cell lines maintained in identical recipients for many months will indicate the degree of functional loss intrinsically timed within precursor cell lines. In the second objective, intact immune organ grafts from aged or younger donors will be transplanted into identical recipients. If defects develop in old but not in young organs, this would suggest functional loss intrinsically timed within organ microenvironments. In the third objective, defective immune responsiveness will be studied in aged mice, some of which will receive precursor cells and intact organs from young donors. Permanently improved immune function in these recipients would indicate that the recipients' own cells and organs had declined with age according to their own intrinsic timing and not solely as the result of general internal deficiencies within the aging individual. Only healthy aged mice will be used. BIBLIOGRAPHIC REFERENCES: Astle, C. M., and D. E. Harrison. 1976. Mitogen synergism in low responding CBA/CaJ mice. Cell Immunol. 21:192-197. Harrison, D. E., and M. Cherry. 1975. Survival of marrow allografts in W/Wv anemic mice: effect of disparity at the Ea-Z locus. Immunogenetics 2: 219-229.